Biology subjects

Harris, M.

Publications and source records attributed to Harris, M..

At least 55 records · Page 3Linked to original sources

bioRxiv2022

Temperature impacts on dengue incidence are nonlinear and mediated by climatic and socioeconomic factors

Temperature can influence mosquito-borne diseases like dengue. These effects are expected to vary geographically and over time in both magnitude and direction and may interact with other environmental variables, making it difficult to anticipate changes in response to climate change. Here, we investigate global variation in temperature-dengue relationship by analyzing published correlations between temperature and dengue and matching them with remotely sensed climatic and socioeconomic data. We found that the correlation between temperature and dengue was most positive at intermediate (near 24{degrees}C) temperatures, as predicted from the thermal biology of the mosquito and virus. Positive temperature-dengue associations were strongest when temperature variation and population density were high and decreased with infection burden and rainfall mean and variation, suggesting alternative limiting factors on transmission. Our results show that while climate effects on diseases are context-dependent they are also predictable from the thermal biology of transmission and its environmental and social mediators.

ecology↗

bioRxiv2022

Contrasting the tempo and mode of adaptation on the X and autosomes in Drosophila melanogaster

The characteristic properties of the X chromosome, such as male hemizygosity and its unique inheritance pattern, expose it to natural selection in a way that can be different from the autosomes. Here, we investigate the differences in the tempo and mode of adaptation on the X chromosome and autosomes in a population of Drosophila melanogaster. Specifically, we test the hypothesis that due to hemizygosity and a lower effective population size on the X, the relative proportion of hard sweeps, which are expected when adaptation is gradual, compared to soft sweeps, which are expected when adaptation is rapid, is greater on the X than on the autosomes. We quantify the incidence of hard versus soft sweeps in North American D. melanogaster population genomic data with haplotype homozygosity statistics and find an enrichment of the proportion of hard versus soft sweeps on the X chromosome compared to the autosomes, confirming predictions we make from simulations. Understanding these differences may enable a deeper understanding of how important phenotypes arise as well as the impact of fundamental evolutionary parameters on adaptation, such as dominance, sex-specific selection, and sex-biased demography.

evolutionary biology↗

bioRxiv2022

Positive strand RNA viruses differ in the constraints they place on the folding of their negative strand

Genome replication of positive strand RNA viruses requires the production of a complementary negative strand RNA that serves as a template for synthesis of more positive strand progeny. Structural RNA elements are important for genome replication, but while they are readily observed in the positive strand, evidence of their existence in the negative strand is more limited. We hypothesised that this was due to viruses differing in their capacity to allow this latter RNA to adopt structural folds. To investigate this, ribozymes were introduced into the negative strand of different viral constructs; the expectation being that if RNA folding occurred, negative strand cleavage and suppression of replication would be seen. Indeed this was what happened with hepatitis C virus (HCV) and feline calicivirus (FCV) constructs. However, little or no impact was observed for chikungunya virus (CHIKV), human rhinovirus (HRV), hepatitis E virus (HEV) and yellow fever virus (YFV) constructs. Reduced cleavage in the negative strand proved to be due to duplex formation with the positive strand. Interestingly, ribozyme-containing RNAs also remained intact when produced in vitro by the HCV polymerase, again due to duplex formation. Overall, our results show that there are important differences in the conformational constraints imposed on the folding of the negative strand between different positive strand RNA viruses.

microbiology↗

bioRxiv2021

Enhancement of alphavirus replication in mammalian cells at sub-physiological temperatures

Chikungunya virus (CHIKV) is an alphavirus transmitted by Aedes mosquitoes, causing fever, rash and arthralgia in mammals. The function of the CHIKV non-structural protein 3 (nsP3) remains enigmatic. Building on previous studies (Gao et al, 2019) [1], we generated a panel of mutants in a conserved and surface-exposed cluster in the nsP3 alphavirus unique domain (AUD) and tested their replication using a sub-genomic replicon (SGR). Three of these SGR mutants replicated well in mosquito cells but poorly in mammalian cells. We observed that this difference was due to culture temperature (mosquito cells: 28{degrees}C; mammalian cells: 37{degrees}C), as the mutants exhibited no replication defect in mammalian cells grown at a sub-physiological temperature (28{degrees}C). Similar phenotypes were observed for infectious CHIKV and the closely related ONyong Nyong virus. Intriguingly, the wildtype SGR replicated more efficiently in mammalian cells at 28{degrees}C compared to 37{degrees}C. To explore the mechanism behind this difference, we focused on two known antiviral pathways: interferon-stimulated genes (ISGs) and stress granules (SGs). SGR replication was concomitant with increased expression of ISGs at 37{degrees}C, but this response was impaired at 28{degrees}C. We also observed enhanced recruitment of the SG component G3BP1 into cytoplasmic sites of viral genome replication at 28{degrees}C. These findings may have real-world implications as when a mosquito bites a mammal, the virus first infects cells in peripheral tissues which are often at sub-physiological temperatures. We propose that alphaviruses such as CHIKV have evolved mechanisms to both promote viral genome replication and concomitantly limit antiviral responses in these cells. Significance statementChikungunya virus (CHIKV) is a re-emerging arbovirus that is transmitted by Aedes mosquitos and poses epidemic threats. Arboviruses must be able to grow efficiently in both the mosquito vector and the mammalian host, which have different body temperatures. Following a mosquito bite, the first cells infected are typically in the skin and are at sub-physiological temperatures, ie lower than the internal body temperature (37{degrees}C). Here we show that CHIKV grows more efficiently in mammalian cells cultured at 28{degrees}C, compared to 37{degrees}C. We investigated the mechanism behind this increase in growth efficiency and demonstrated that at the lower temperature the production of antiviral genes was impaired. Additionally, proteins that respond to cellular stress and are needed for virus replication were more abundantly recruited to sites in the cell where the virus was replicating. We propose that CHIKV has evolved mechanisms to promote its replication in mammalian cells at sub-physiological temperatures to facilitate infection of mammals via a mosquito bite.

microbiology↗

bioRxiv2021

Genomic sequence characteristics and the empiric accuracy of short-read sequencing

BackgroundShort-read whole genome sequencing (WGS) is a vital tool for clinical applications and basic research. Genetic divergence from the reference genome, repetitive sequences, and sequencing bias, reduce the performance of variant calling using short-read alignment, but the loss in recall and specificity has not been adequately characterized. For the clonal pathogen Mycobacterium tuberculosis (Mtb), researchers frequently exclude 10.7% of the genome believed to be repetitive and prone to erroneous variant calls. To benchmark short-read variant calling, we used 36 diverse clinical Mtb isolates dually sequenced with Illumina short-reads and PacBio long-reads. We systematically study the short-read variant calling accuracy and the influence of sequence uniqueness, reference bias, and GC content. [a] ResultsReference based Illumina variant calling had a recall [≥]89.0% and precision [≥]98.5% across parameters evaluated. The best balance between precision and recall was achieved by tuning the mapping quality (MQ) threshold, i.e. confidence of the read mapping (recall 85.8%, precision 99.1% at MQ [≥] 40). Masking repetitive sequence content is an alternative conservative approach to variant calling that maintains high precision (recall 70.2%, precision 99.6% at MQ[≥]40). Of the genomic positions typically excluded for Mtb, 68% are accurately called using Illumina WGS including 52 of the 168 PE/PPE genes (34.5%). We present a refined list of low confidence regions and examine the largest sources of variant calling error. ConclusionsOur improved approach to variant calling has broad implications for the use of WGS in the study of Mtb biology, inference of transmission in public health surveillance systems, and more generally for WGS applications in other organisms.

bioinformatics↗

bioRxiv2021

RAMPs regulate signalling bias and internalisation of the GIPR

Gastric inhibitory polypeptide (GIP) receptor is a class B1 GPCR, that responds to GIP and physiologically potentiates glucose-stimulated insulin secretion. Like most class B1 GPCRs, GIPR has been shown to interact with RAMPs, yet the effects of RAMPs on its signalling and trafficking remain poorly understood. We demonstrate that RAMPs modulate G protein activation and GIPR internalisation profiles. RAMP3 reduced GIPR Gs activation and cAMP production but retained GIPR at the cell surface, and this was associated with prolonged ERK1/2 phosphorylation and {beta}-arrestin association. By contrast, RAMP1/2 reduced Gq/11/15 activation of the GIPR. Through knockout mice studies, we show that RAMP1 is important to the normal physiological functioning of GIPR to regulate blood glucose levels. Thus, RAMPs act on G protein/{beta}-arrestin complexes, having both acute and chronic effects on GIPR function, while this study also raises the possibility of a more general role of RAMP3 to enhance GPCR plasma membrane localisation.

pharmacology and toxicology↗

bioRxiv2021

Refining Convergent Rate Analysis with Topology in Mammalian Longevity and Marine Transitions

The quest to map the genetic foundations of phenotypes has been empowered by the modern diversity, quality, and availability of genomic resources. Despite these expanding resources, the abundance of variation within lineages makes the association of genetic change to specific phenotypes improbable. Drawing such connections requires an a priori means of isolating the associated changes from background genomic variation. Evolution may provide these means via convergence; i.e., the shared variation that may result from replicate evolutionary experiments across independent trait occurrences. To leverage these opportunities, we developed TRACCER: Topologically Ranked Analysis of Convergence via Comparative Evolutionary Rates. As compared to current methods, this software empowers rate convergence analysis by factoring in topological relationships, because variation between phylogenetically proximate trait changes is more likely to be facilitating the trait. Pairwise comparisons are performed not with singular branches, but in reference to their most recent common ancestors. This ensures that comparisons represent identical genetic contexts and timeframes while obviating the problematic requirement of assigning ancestral states. We applied TRACCER to two case studies: marine mammal transitions, an unambiguous trait which has independently evolved three times, as well as the evolution of mammalian longevity, a less delineated trait but with more instances to compare. TRACCER, by factoring in topology, identifies highly significant, convergent genetic signals in these test cases, with important incongruities and statistical resolution when compared to existing convergence approaches. These improvements in sensitivity and specificity generate refined targets for downstream analysis of convergent evolution and identification of genotype-phenotype relationships.

genomics↗

bioRxiv2021

Identification of host antiviral genes differentially induced by clinically diverse strains of Tick-Borne Encephalitis Virus

Tick Borne Encephalitis Virus (TBEV) is an important human arthropod-borne virus, which causes tick-borne encephalitis (TBE), an acute viral infection of the central nervous system (CNS) that causes neurological symptoms of varying severity. TBEV is prevalent in large parts of central- and northern-Europe as well as Northern Asia, and strains of varying pathogenicity have been described. Both host and viral specific characteristics have been postulated to determine the outcome of TBEV infection, but the exact basis of their clinical variability remains undefined. Here, we report the generation of Spinach RNA aptamer labelled TBEV replicons of high (Hypr) and low (Vs) pathogenicity isolates and perform the first direct comparison of both strains in cell culture. We show that pathogenic Hypr replicates to higher levels than Vs in mammalian cells, but not in arthropod cells, and that the basis of this difference maps to the NS5 region, encoding the methyltransferase and RNA polymerase. For both Hypr and Vs strains, NS5 and the viral genome localized to defined intracellular structures typical of positive strand RNA viruses, but Hypr was associated with significant activation of IRF-3, caspase-3 and caspase-8, whilst Vs activated Akt, affording protection against caspase-mediated apoptosis. Activation of TIAR and the formation of cytoplasmic stress granules were an additional early feature of Vs but not Hypr replication. Taken together, these findings highlight NS5 and novel host cell responses as key underling factors for the differential clinical characteristics of TBEV strains. ImportanceTick-borne encephalitis virus (TBEV) is an emerging virus of the flavivirus family spread by ticks. Tick bite can transfer the virus and lead to a febrile infection, Tick-borne encephalitis, of varying severity. There is no specific therapeutic treatment and control in endemic areas is by vaccination. The basis of the different pathologies shown following TBEV infection, from mild to fatal, is not clear although the virus genotype clearly has a role. Mapping the basis of their differential effects would allow focus on the stages of the replication cycle responsible, which might guide the development of therapeutic interventions or the creation of purposefully attenuated strains as candidate vaccines.

microbiology↗

bioRxiv2020

Higher-order structures of the foot-and-mouth disease virus RNA-dependent RNA polymerase required for dynamic inter-molecular interactions involved in viral genome replication

Replication of many positive-sense RNA viruses occurs within intracellular membrane-associated compartments. These are believed to provide a favourable environment for replication to occur, concentrating essential viral structural and non-structural components, as well as protecting these components from host-cell pathogen recognition and innate immune responses. However, the details of the molecular interactions and dynamics within these structures is very limited. One of the key components of the replication machinery is the RNA-dependent RNA polymerase, RdRp. This enzyme has been shown to form higher-order fibrils in vitro. Here, using the RdRp from foot-and-mouth disease virus (termed 3Dpol), we report fibril structures, solved at ~7-9 [A] resolution by cryo-EM, revealing multiple conformations of a flexible assembly. Fitting high-resolution coordinates led to the definition of potential intermolecular interactions. We employed mutagenesis using a sub-genomic replicon system to probe the importance of these interactions for replication. We use these data to propose models for the role of higher order 3Dpol complexes as a dynamic scaffold within which RNA replication can occur.

microbiology↗

bioRxiv2020

Intra- and extra-cellular environments contribute to the fate of HIV-1 infection

HIV-1 entry into host cells leads to one of three alternative fates: 1) HIV-1 elimination by restriction factors, 2) establishment of HIV-1 latency, or 3) active viral replication in target cells. Here we developed an improved system for monitoring HIV-1 fate and provide evidence for the differential contribution of the intracellular environment as well as extracellular environment found in organs of BLT humanized mouse to the fate of HIV-1 infection.

microbiology↗

bioRxiv2020

Cocaine-induced neuron subtype mitochondrial dynamics through Egr3 transcriptional regulation

Mitochondrial function is required for brain energy homeostasis and neuroadaptation. Recent studies demonstrate that cocaine affects mitochondrial dynamics and morphological characteristics within the nucleus accumbens (NAc). Further, mitochondria are differentially regulated by cocaine in dopamine receptor-1 containing medium spiny neurons (D1-MSNs) vs dopamine receptor-2 (D2)-MSNs. However, there is little understanding into cocaine-induced transcriptional mechanisms and their role in regulating mitochondrial processes. Here, we demonstrate that cocaine enhances binding of the transcription factor, early growth response factor 3 (Egr3), to nuclear genes involved in mitochondrial function and dynamics. Moreover, cocaine exposure regulates mRNA of these mitochondria-associated nuclear genes in both contingent or noncontingent cocaine administration and in both rodent models and human postmortem tissue. Interestingly, several mitochondrial nuclear genes showed distinct profiles of expression in D1-MSNs vs D2-MSNs, with cocaine exposure generally increasing mitochondrial-associated nuclear gene expression in D1-MSNs vs suppression in D2-MSNs. We further show that blunting Egr3 expression in D1-MSNs blocks cocaine-enhancement of the mitochondrial-associated transcriptional coactivator, peroxisome proliferator-activated receptor gamma coactivator (PGC1), and the mitochondrial fission molecule, dynamin related protein 1 (Drp1). Finally, reduction of D1-MSN Egr3 expression attenuates cocaine-induced enhancement of small-sized mitochondria, causally demonstrating that Egr3 regulates mitochondrial morphological adaptations. Collectively, these studies demonstrate cocaine exposure impacts mitochondrial dynamics and morphology by Egr3 transcriptional regulation of mitochondria-related nuclear gene transcripts; indicating roles for these molecular mechanisms in neuronal function and plasticity occurring with cocaine exposure.

neuroscience↗

bioRxiv2020

HIV Diversity Considerations in the Application of the Intact Proviral DNA Assay (IPDA)

Opening Paragraph (serves as abstract for submission) and BodyThe Intact Proviral DNA Assay (IPDA) was developed to address the critical need for a precise and scalable method for intact HIV reservoir quantification1. This duplexed droplet digital PCR (ddPCR) assay simultaneously targets the HIV Packaging Signal ({Psi}) and the Rev Responsive Element (RRE) within Envelope (env) to distinguish genomically intact proviruses against a large background of defective ones2. The IPDA requires less time, resources, and biological material than the gold standard for replication-competent HIV reservoir measurement, the Quantitative Viral Outgrowth Assay (QVOA)3, and is being adopted in research and clinical studies4-7. In our cohort of HIV-1 subtype B-infected individuals from North America however, the IPDA yielded a 28% failure rate due to HIV polymorphism. We further demonstrate that within-host HIV diversity can lead the IPDA to underestimate intact HIV reservoir size, which could negatively impact clinical trial results interpretation. While the IPDA represents an important methodological advance, HIV diversity should be addressed before its widespread adoption.

genetics↗

bioRxiv2020

Single-cell analysis reveals mechanisms of plasticity of leukemia initiating cells

Leukemia initiating cells (LICs) fuel leukemic growth and spark relapse. Previously thought to be primitive and rare, the LIC state may actually be heterogeneous and dynamic, enabling evasion of therapies. Here, we use single-cell transcriptomics to track LIC multipotency within the cellular ontogeny of MLL-rearranged B-lymphoblastic leukemia (MLL-r B-ALL). Although we identify rare transcriptionally and phenotypically primitive LICs, we also observe LICs emerging from more differentiated populations with the capability to replenish the full leukemic cellular diversity. We find that activation of MYC-driven oxidative phosphorylation controls this process of facultative state conversion in LICs.

cancer biology↗

bioRxiv2019

Prediction of multiple drug resistant pulmonary tuberculosis against drug sensitive pulmonary tuberculosis by CT nodular consolidation sign

Multidrug-resistant tuberculosis (mdrtb) refers to TB infection resistant to at least two most powerful anti-TB drugs, isoniazid and rifampincin. It has been estimated that globally 3.5% (which can be much higher in some regions) of newly diagnosed TB patients, and 20.5% of previously treated patients had mdrtb. Extensively drug-resistant TB (xdrtb) has resistance to rifampin and isoniazid, as well as to any member of the quinolone family and at least one of the second line injectable drugs: kanamycin, amikacin and capreomycin. xdrtb accounts for 4-20% of mdrtb. Early detection and targeted treatment are priorities for mdrtb/xdrtb control. The suspicion of mdr/xdr -pulmonary TB (mdrptb or xdrptb) by chest imaging shall suggest intensive diagnostic testing for mdrptb/xdrptb. We hypothesize that multiple nodular consolidation (NC) may serve one of the differentiators for separating dsptb vs mdrptb/xdrptb cases. For this study, mdrptb cases (n=310) and XDR-PTB cases ([xcap]=I58) were from the NIAID TB Portals Program (TBPP) . Drug sensitive pulmonary TB (dsptb) cases were from the TBPP collection (n=112) as well as the Shenzhen Center for Chronic Disease Control (n=111), Shenzhen, China, and we excluded patients with HIV(+) status. Our study shows NC, particularly multiple NCs, is more common in mdrptb than in dsptb, and more common in xdrptb than in mdrptb. For example, 2.24% of dsptb patients, 13.23% of mdrptb patients, and 20.89% of xdrptb patients, respectively, have NCs with diameter >= 10mm equal or more than 2 in number.

pathology↗

bioRxiv2019

Promiscuous receptor activation mediates glucagonostatic effects of GLP-1(9-36) and GLP-1(7-36)

The incretin hormone glucagon-like peptide 1(7-36) (GLP-1(7-36)) stimulates insulin and inhibits glucagon secretion. The mechanisms by which GLP-1 suppresses glucagon release are unclear as glucagon-secreting -cells express GLP-1 receptors (GLP-1Rs) at very low levels. Here, we examine the underlying mechanisms. We find that both GLP-1(7-36) and its degradation product GLP-1(9-36) inhibit glucagon secretion at physiological (pM) concentrations. Whereas the effect of GLP-1(7-36) is sensitive to PKA inhibition, GLP-1(9-36) exerts its effect by a PKA-independent mechanism sensitive to pretreatment with pertussis. The glucagonostatic effects of both GLP-1(7-36) and (9-36) are retained in islets from Glp1r knockout mice but only GLP-1(9-36) remains glucagonostatic in the presence of the DPP-4 (the peptidase catalyzing the formation of GLP-1(9-36)) inhibitor sitagliptin. Glucagon receptor (GCGR) antagonism specifically prevents the inhibitory effects of GLP-1(9-36) whilst not affecting that of GLP-1(7-36). We conclude that GLP-1(7-36) and GLP-1(9-36) regulate glucagon secretion via interaction with GLP-1R and GCGR, respectively. HighlightsO_LIGLP-1(7-36) and GLP-1(9-36) inhibit glucagon secretion from alpha-cells C_LIO_LIGLP-1(7-36) and (9-36) retain glucagonostatic effect in Glp1r-/- islets C_LIO_LIGLP-1(7-36) and (9-36) activate distinct signal transduction mechanisms C_LIO_LIGLP-1(7-36) acts via GLP-1R and GLP-1(9-36) via GCGR C_LI

molecular biology↗

bioRxiv2019

The Chikungunya virus nsP3 macro domain inhibits activation of the NF-κB pathway

The role of the chikungunya virus (CHIKV) non-structural protein 3 (nsP3) in the virus lifecycle is poorly understood. The protein comprises 3 domains. The N-terminus is a macro domain, biochemically characterised to bind both RNA and ADP-ribose, and to possess ADP-ribosyl hydrolase activity - an enzymatic activity that removes ADP-ribose from mono-ADP-ribosylated proteins. As ADP-ribosylation is important in the signalling pathway leading to activation of the transcription factor NF-{kappa}B, we sought to determine if the macro domain might perturb NF-{kappa}B signalling. We first show that CHIKV infection did not induce NF-{kappa}B activation, and could not block exogenous activation of the pathway via TNF, although TNF treatment did reduce virus titres. Ectopic expression of nsP3 was able to block TNF-mediated NF-{kappa}B activation and this was dependent on the macro domain, as mutations previously shown to disrupt either ADP-ribose binding or hydrolase activity lost the ability to inhibit NF-{kappa}B activation. Lastly, we determined the phenotype of the macro domain mutants in the context of virus infection in a range of cell types. Our data are consistent with cell- and species-dependent roles of the macro domain, however, these phenotypes do not correlate with the ability to inhibit NF-{kappa}B activation suggesting that the macro domain plays multiple independent roles in the virus lifecycle.

microbiology↗

bioRxiv2019

Elevated intracellular cAMP concentration mediates growth suppression in glioma cells

Supressed levels of intracellular cAMP have been associated with malignancy. Thus, elevating cAMP through activation of adenylyl cyclase (AC) or by inhibition of phosphodiesterase (PDE) may be therapeutically beneficial. Here, we demonstrate that elevated cAMP levels suppress growth in C6 cells (a model of glioma) through treatment with forskolin, an AC activator, or a range of small molecule PDE inhibitors with differing selectivity profiles. Forskolin suppressed cell growth in a protein kinase A (PKA)-dependent manner by inducing a G2/M phase cell cycle arrest. In contrast, trequinsin (a non-selective PDE2/3/7 inhibitor), not only inhibited cell growth via PKA, but also stimulated (independent of PKA) caspase-3/-7 and induced an aneuploidy phenotype. Interestingly, a cocktail of individual PDE 2,3,7 inhibitors suppressed cell growth in a manner analogous to forskolin but not trequinsin. Finally, we demonstrate that concomitant targeting of both AC and PDEs synergistically elevated intracellular cAMP levels thereby potentiating their antiproliferative actions.

pharmacology and toxicology↗

bioRxiv2019

The Dreem Headband as an Alternative to Polysomnography for EEG Signal Acquisition and Sleep Staging

Despite the central role of sleep in our lives and the high prevalence of sleep disorders, sleep is still poorly understood. The development of ambulatory technologies capable of monitoring brain activity during sleep longitudinally is critical to advancing sleep science and facilitating the diagnosis of sleep disorders. We introduced the Dreem headband (DH) as an affordable, comfortable, and user-friendly alternative to polysomnography (PSG). The purpose of this study was to assess the signal acquisition of the DH and the performance of its embedded automatic sleep staging algorithms compared to the gold-standard clinical PSG scored by 5 sleep experts. Thirty-one subjects completed an over-night sleep study at a sleep center while wearing both a PSG and the DH simultaneously. We assessed 1) the EEG signal quality between the DH and the PSG, 2) the heart rate, breathing frequency, and respiration rate variability (RRV) agreement between the DH and the PSG, and 3) the performance of the DHs automatic sleep staging according to AASM guidelines vs. PSG sleep experts manual scoring. Results demonstrate a strong correlation between the EEG signals acquired by the DH and those from the PSG, and the signals acquired by the DH enable monitoring of alpha (r= 0.71 {+/-} 0.13), beta (r= 0.71 {+/-} 0.18), delta (r = 0.76 {+/-} 0.14), and theta (r = 0.61 {+/-} 0.12) frequencies during sleep. The mean absolute error for heart rate, breathing frequency and RRV was 1.2 {+/-} 0.5 bpm, 0.3 {+/-} 0.2 cpm and 3.2 {+/-} 0.6 %, respectively. Automatic Sleep Staging reached an overall accuracy of 83.5 {+/-} 6.4% (F1 score : 83.8 {+/-} 6.3) for the DH to be compared with an average of 86.4 {+/-} 8.0% (F1 score: 86.3 {+/-} 7.4) for the five sleep experts. These results demonstrate the capacity of the DH to both precisely monitor sleep-related physiological signals and process them accurately into sleep stages. This device paves the way for high-quality, large-scale, longitudinal sleep studies.

neuroscience↗